Comparison of geriatric nutritional risk index and creatinine index in short-term mortality prediction in maintenance hemodialysis patients.

BACKGROUND: The aim of this study is to analyze and compare the predictive values of the Geriatric Nutritional Risk Index (GNRI) and Creatinine Index (CI) in the short-term mortality of maintenance hemodialysis patients and to determine their best cut-offs. METHODS: A total of 169 adult hemodialysis patients were included in this retrospective, cross-sectional, and single-center study. The demographic, clinical, and laboratory data of the month in which the patients were included in the study were obtained from their medical files and computer records. All-cause death was the primary outcome of the study during a 12-month follow-up after baseline GNRI and CI calculations. RESULTS: The mean age of the study population was 57 ± 16 years (49.7% were women, 15% were diabetic). During the one-year observation period, 19 (11.24%) of the cases died (8 CV deaths). The optimal cut-off value for GNRI was determined as 104.2 by ROC analysis [AUC = 0.682 ± 0.06, (95% CI, 0.549-0.815), p = 0.01]. The low GNRI group had a higher risk for all-cause and CV mortality compared to the higher GNRI group (p = 0.02 for both in log-rank test). The optimal sex-specific cut-off was 12.18 mg/kg/day for men [AUC = 0.723 ± 0.07, (95% CI, 0.574-0.875), p = 0.03] and was 12.08 mg/kg/day for females [AUC = 0.649 ± 0.13, (95% CI, 0.384- 0.914), p = 0.01]. Patients with lower sex-specific CI values had higher all-cause and CV mortality (p = 0.001 and p = 0.009 in log-rank test, respectively). In multivariate cox models, both GNRI [HR = 4.904 (% 95 CI, 1.77-13.56), p = 0.002] and sex-specific CI [HR = 5.1 (95% CI, 1.38-18.9), p = 0.01] predicted all-cause mortality. The association of GNRI with CV was lost [HR = 2.6 (CI 95%, 0.54-13.455), p = 0.22], but low CI had a very strong association with CV mortality [HR = 11.48 (CI 95%, 1.25 -104), p = 0.03]. DISCUSSION: In hemodialysis patients, GNRI and CI have similar powers in predicting all-cause short-term mortality. The association of CI with all-cause death depends on gender. On the other hand, sex-specific CI predicts CV mortality better than GNRI.

COVID-19 infection in a kidney transplant recipient-special emphasis on pharmacokinetic interactions: A case report.

BACKGROUND: Solid organ transplant recipients are considered to be at high-risk of developing coronavirus disease 2019 (COVID-19)-related complications. The optimal treatment for this patient group is unknown. Consequently, the treatment of COVID-19 in kidney transplant recipients should be determined individually, considering patient age and comorbidities, as well as graft function, time of transplant, and immunosuppressive treatment. Immunosuppressive treatments may give rise to severe COVID-19. On the contrary, they may also lead to a milder and atypical presentation by diminishing the immune system overdrive. CASE SUMMARY: A 50-year old female kidney transplant recipient presented to the transplant clinic with a progressive dry cough and fever that started three days ago. Although the COVID-19 test was found to be negative, chest computed tomography images showed consolidation typical of the disease; thus, following hospital admission, anti-bacterial and COVID-19 treatments were initiated. However, despite clinical improvement of the lung consolidation, her creatinine levels continued to increase. Ultrasound of the graft showed no pathology. The tacrolimus blood level was determined and the elevation in creatinine was found to be related to an interaction between tacrolimus and azithromycin. CONCLUSION: During the COVID-19 pandemic, various single or combination drugs have been utilized to find an effective treatment regimen. This has increased the possibility of drug interactions. A limited number of studies published in the literature have highlighted some of these pharmacokinetic interactions. Treatments used for COVID-19 therapy; azithromycin, atazanavir, lopinavir/ritonavir, remdesivir, favipiravir, chloroquine, hydroxychloroquine, nitazoxanide, ribavirin, and tocilizumab, interact with immunosuppressive treatments, most importantly with calcineurin inhibitors. Thus, their levels should be frequently monitored to prevent toxicity.

Association of neutrophil-to-lymphocyte ratio and microalbuminuria in patients with normal eGFR.

AIMS: The aim of this study was to evaluate the association between neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and microalbuminuria in patients with normal estimated glomerular filtration rate (eGFR). METHODS: 174 patients who had eGFR ≥ 60 mL/min/1.73 m2 were studied. Patients were divided into two groups according to the urinary albumin excretion as microalbuminuric group (n = 105) and normoalbuminuric group (n = 69). NLR and PLR levels were calculated. RESULTS: NLR was significantly higher (p < 0.05) in microalbuminuric patients (1.91 ± 0.70) compared with normoalbuminuric patients (1.63 ± 0.53). A positive correlation was found between urine albumin excretion and NLR in the whole study group (r = 0.214, p < 0.005). CONCLUSIONS: Higher NLR levels were found in microalbuminuric patients with normal eGFR. Also a significant positive correlation was observed between albuminuria and NLR.

Epicardial Adiposity is Associated with Microalbuminuria in Patients with Essential Hypertension.

BACKGROUND: Measurement of epicardial adipose tissue (EAT) is suggested as a novel cardiometabolic risk factor. Microalbuminuria is a marker of endothelial dysfunction and is associated with an increased risk for cardiovascular disease in patients with systemic hypertension. The aim of this study was to investigate the relationship of echocardiographic epicardial adipose tissue (EAT) thickness and microalbuminuria in hypertensive patients. METHODS: 75 essential hypertensive patients were included into the study. All subjects underwent transthoracic echocardiography to measure EAT thickness. Spot urine sample was collected for the assessment of microalbuminuria. Patients were divided into two groups according to their spot urine albumin to creatinine ratio (UACR); Group 1 included normoalbuminuria (0-30 µg/mg); and Group 2: included microalbuminuria (30-300 µg/mg). Thereafter, we evaluated patient characteristics including smoking status, blood pressure, body mass index (BMI), antihypertensive treatment, statin therapy and serum levels of total cholesterol, low-density lipoprotein cholesterol, triglicerides, albumin, C-reactive protein (CRP), creatinine and hemoglobin. RESULTS: There was no difference in baseline characteristics between Group 1 and Group 2. Patients with microalbuminuria had significantly higher mean EAT thickness values compared to the normoalbuminuria group (7.1 ± 0.9 vs. 6.6 ± 0.9, p = 0.01). There were positive significant correlations between EAT and age (r = 0.267, p = 0.020), serum creatinine (r = 0.292, p = 0.01), UACR (r = 0.251, p = 0.03), left ventricular mass (r = 0.257, p = 0.03) and left ventricular mass index (r = 0.242, p = 0.04). UACR was independently associated with EAT (p = 0.01) after adjustments were made for age and BMI. CONCLUSIONS: Epicardial Adipose Tissue (EAT) thickness could be associated with microalbuminuria in patients with essential hypertension. This association could support the recognition of EAT as a credible marker in cardiovascular risk stratification.

Protective effect of beta-glucan on contrast induced-nephropathy and a comparison of beta-glucan with nebivolol and N-acetylcysteine in rats.

BACKGROUND: It has been shown that beta-glucan (BG), which has antioxidant and immunomodulatory effects, attenuats renal ischemia-reperfusion injury. We aimed to investigate whether BG might have a preventive role against the development of contrast-induced nephropathy and to compare its effect with nebivolol (Nb) and N-acetylcysteine (NAC). METHODS: Thirty-six Wistar albino female rats were randomly divided into six groups (n = 6 each): control, contrast media (CM), BG, BG + CM, Nb + CM, and NAC + CM. With the exception of control and CM groups, the others were given drugs orally once a day for 5 days. Kidney function parameters, inflammatory parameters, and serum and renal tissue oxidative stress markers were measured. RESULTS: Increases of serum creatinine and blood urea nitrogen levels were significantly higher (p < 0.05) in the CM group only. Absolute changes of serum creatinine levels in BG, BG + CM and Nb + CM groups were significantly lower than those in the CM group (p < 0.05). Serum levels of advanced oxidation protein products and malondialdehyde were significantly less (p < 0.05) in the BG group compared to the CM group. Histopathological lesions in the CM group were more advanced (p < 0.05). No significant differences between the BG + CM, Nb + CM and NAC + CM groups were found with regard to histopathological findings. CONCLUSION: This study suggests that BG protects or ameliorates against contrast-induced nephropathy. Its beneficial effects may be similar to or greater than those of Nb or NAC.

Association of the angiotensinogen M235T and APO E gene polymorphisms in Turkish type 2 diabetic patients with and without nephropathy.

BACKGROUND: Diabetic nephropathy (DN) is a leading cause of diabetes-related morbidity and mortality. The aim of this study was to evaluate the relationship of AGT M235T and apoprotein E (APO E) gene polymorphism with DN in Turkish patients of Type 2 diabetes, and to compare genotype and allele distributions among DN patients, non-DN patients, and healthy controls. METHODS: AGT M235T and APO E genotype and allele analysis were performed in 111 DN patients, 108 non-DN patients, 106 healthy control subjects for APO E genotype, and 100 for AGT M235T genotype polymorphism. APO E and AGT M235T genotype were determined by RFLP-PCR. RESULTS: The frequencies of APO E ε2/3, ε 3/3, ε 3/4 genotypes were 22.7%, 60%, 60%, respectively, among DN patients and 6.6%, 80%, 10.4%, respectively (p < 0.001), in the non-DN patients. The frequencies of AGT M235T MM, MT, TT genotypes among the same groups were 17%, 46%, 37% and 21%, 63%, 16%, respectively (p < 0.02). Having the ε2/3 genotype and TT genotype increased the risk for DN nephropathy [4.8-fold (95% CI: 1.94-11.67), 2.9-fold (95% CI: 1.27-6.69), respectively]. CONCLUSION: Our study has shown that AGT M235T TT genotype and APO E ε 2/3 genotype may be linked to a risk for DN among Turkish population.

Could nephrotoxicity due to colistin be ameliorated with the use of N-acetylcysteine?

PURPOSE: The protective effect of N-acetylcysteine (NAC) on nephrotoxicity due to contrast nephropathy and reperfusion-induced ischemia has been reported in experimental models. However, its efficacy on colistin-induced nephrotoxicity has not been elucidated yet. The primary aim of this study was to evaluate the nephrotoxic effect of colistin and to investigate the possible protective effect of NAC on colistin-induced nephrotoxicity. The secondary aim was to research the systemic effects of nephrotoxicity-induced oxidative stress on the lung. METHODS: Eighteen female Sprague-Dawley rats were randomly assigned and were given (a) 1 ml/kg sterile saline, (b) 300,000 IU/kg/day colistin, and (c) 300,000 IU/kg/day colistin and 150 mg/kg NAC for six consecutive days. RESULTS: Plasma blood urea nitrogen (BUN), creatinine, urinary creatinine, urinary protein, plasma TNF-alpha levels, renal tissue superoxide dismutase (SOD) and malondialdehyde (MDA) activity and immunocytochemical findings were evaluated. Colistin exerted nephrotoxicity and achieved a significant increase in plasma BUN and creatinine levels and renal tissue SOD levels. NAC exhibited no significant effect on biochemical parameters but reduced renal tissue SOD level and reversed immunocytochemical staining of inducible nitric oxide synthase (i-NOS) and neurotrophin-3. Increased oxidative stress in the lung tissue of the rats treated with colistin has also been documented. Additionally, NAC significantly reduced the immunostaining of endothelial NOS (e-NOS) and i-NOS in the lung tissue. CONCLUSIONS: Colistin-induced renal toxicity may be attributable to oxidative damage. The combined treatment of colistin plus NAC seems to have a beneficial role in restoration of the oxidant injury which may be related to its antioxidant effect.

A spontaneous spinal epidural hematoma in a hemodialysis patient: a rare entity.

Hemodialysis patients are at an increased risk of bleeding due to the platelet dysfunction caused by uremia and the use of anticoagulants during dialysis. Spontaneous spinal hematoma is a rare disorder as a complication in hemodialysis patients. Also it includes the hematoma secondary to coagulopathy, vascular malformation and hemorrhagic tumors. Here, we report the case of 77-year-old woman who presented with spinal cord compression due to spontaneous spinal epidural hematoma associated with hemodialysis. When an end-stage renal disease patient suffers from back pain and neurological deficits, the clinician should be alerted for the spontaneous spinal epidural hematoma as well as cerebrovascular events.

Renal cell carcinoma associated immunosuppressive therapy: a case report with Wegener's granulomatosis.

Development of uroepithelial tumors after cyclophosphamide and azathioprine therapy in Wegener's granulomatosis (WG) have been reported in the literature but renal cell carcinoma (RCC), rarely. RCC associated with WG has been previously reported in a few cases. Most of them have simultaneous diseases. Here, we report a case, which developed RCC 8 years after initiation of WG. Long-term immunosuppressive treatment is a risk factor for the development of malignancies; it should be suggested that RCC in our patient might be due to immunosuppressive therapy.

Does the urinary excretion of alpha1-microglobulin and albumin predict clinical disease activity in ulcerative colitis?

INTRODUCTION: There remains some difficulty in determining disease activity during the development of inflammatory bowel disease (IBD). The excretion levels of some inflammatory response molecules increase as a result of the onset of this disease. We studied urinary alfa-1-microglobulin (alpha1-MG) and albumin levels in patients with active and inactive ulcerative colitis (UC) and investigated whether we could use these parameters as an activity index. METHODS: The study was carried out at Gazi University Faculty of Medicine, Nephrology and Gastroenterology Departments, between December 2003 and March 2006. In total, 35 patients (male/female: 16/19, mean age: 38.3+/-2.4 years) and 13 healthy controls (male/female: 6/7, mean age: 35.8+/-2.8 years) were enrolled in the study. Nineteen patients had symptoms of active disease and the remaining 16 patients had inactive disease. RESULTS: There was a significant difference in serum C-reactive protein (CRP), urinary albumin excretion, and alpha1-MG excretion levels between patients and controls. Patients with active disease had significantly higher serum CRP and alpha1-MG levels than those with inactive disease and controls. Patients with active disease had higher microalbuminuria levels than inactive patients, but this difference was not statistically significant. Urinary albumin and alpha1-MG excretion did not correlate with serum CRP levels. CONCLUSION: The present study suggests that, as with CRP, urinary levels of albumin and alpha1-MG increase during the active period of UC. During the inactive period, concentrations of these parameters are comparable to controls. The measurement of alpha1-MG and/or microalbuminuria could provide information on disease severity and response to treatment.

The relationship of visfatin levels to inflammatory cytokines and left ventricular hypertrophy in hemodialysis and continuous ambulatory peritoneal dialysis patients.

Visfatin was recently defined as an adipocytokine; however, the pathophysiological role of visfatin is not completely understood. A few studies suggest that visfatin may be a new proinflammatory adipocytokine. The aim of the present study was to compare serum visfatin levels between hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) patients and evaluate the relationship between visfatin levels to IL-6, TNF-alpha, and left ventricular hypertrophy. Serum visfatin, IL-6, and TNF-alpha levels were measured by using the ELISA method, and echocardiographic evaluations were performed in 31 hemodialysis patients, 30 CAPD patients, and 21 healthy volunteers. Serum visfatin levels were higher in the CAPD group (265.27 +/- 387.86 ng/mL) than hemodialysis (97.68 +/- 244.96 ng/mL,) and control (41.33 +/- 48.87 ng/mL) groups (p = 0.04, p = 0.01, respectively). No significant difference was observed between the hemodialysis and control groups. In univariate analysis, visfatin levels were positively correlated with IL-6 (r = 0.24, p = 0.03), TNF-alpha (r = 0.34, p = 0.002), and BMI (r = 0.26, p = 0.03) and negatively correlated with some left ventricular diastolic parameters [Em and Em/Am (r = -0.305, p = 0.01), (r = -0.251, p = 0.03), respectively]. No relationship was found between visfatin and left ventricular mass index. In the linear regression analysis, visfatin levels independently related with TNF-( (beta = 0.369, p = 0.001) and IL-6 (beta = 0.284, p = 0.015). This study has found significantly higher levels of serum visfatin in CAPD patients when compared to healthy individuals. Increased visfatin levels seem to associate with proinflammatory cytokines such as IL-6 or TNF-alpha. As for the effects of on left ventricular structure and functions, visfatin might have negative effects on left ventricular diastolic function parameters but have no effects on left ventricular mass index.

The relationship among asymmetric dimethylarginine (ADMA) levels, residual renal function, and left ventricular hypertrophy in continuous ambulatory peritoneal dialysis patients.

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial-based nitric oxide synthase. Its level is increased by end stage renal disease. However, most studies showing an increase in ADMA in dialysis patients have focused on hemodialysis. Results with peritoneal dialysis patients have been more inconclusive. Recent studies suggest that ADMA may be a new cardiovascular risk factor. The aim of the present study was to evaluate the relationship between ADMA levels, residual renal function, and left ventricular hypertrophy in peritoneal dialysis patients. Serum ADMA measurements and echocardiographic evaluations were performed in 54 peritoneal dialysis patients and 26 healthy volunteers. Residual renal function was measured in peritoneal dialysis patients by urea clearance from a urine collection. Thirty-two of the 54 peritoneal dialysis patients had residual renal function. ADMA levels of the peritoneal dialysis group were found to be significantly higher than those of healthy individuals (p = 0.03). Within the peritoneal dialysis group, ADMA levels of patients with residual renal function were significantly lower than those without residual renal function (p = 0.01), though they were still higher than the ADMA levels of the control group (p = 0.04). Serum levels of ADMA were positively correlated with left ventricular mass index (r = 0.29, p = 0.01) and negatively correlated with early mitral inflow velocity (Em) (r = -0.28, p = 0.01), Em/Late mitral inflow velocity (Am) (r = -0,32, p = 0.00), and isovolumetric relaxation time (r = -0.30, p = 0.01). In conclusion, increased ADMA levels seem to be associated with left ventricular hypertrophy in peritoneal dialysis patients, and residual renal function may lead to a reduction of serum ADMA levels.

Impact of adiponectin on left ventricular mass index in non-complicated obese subjects.

To evaluate the relationship between the adiponectin levels and left ventricular mass index (LVMI) in uncomplicated obese subjects. Fifty-nine subjects were assigned to the obese (BMI> or =30 kg/m(2)) and 58 to the lean (BMI<30 kg/m (2) ) group. Plasma glucose, insulin, serum total cholesterol and high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides and adiponectin were measured. Insulin resistance was determined by the Homeostasis Assessment Model (HOMA-IR). The left ventricular functions of all subjects were determined by 2D and pulse wave Doppler echocardiography. LVMI was calculated as left ventricular mass (LVM) normalized for height in m (2.7) . The obese group displayed significantly higher LVMI and late mitral inflow velocity. Thirty-three obese subjects met the criteria for left ventricular hypertrophy (LVH) and had lower serum adiponectin levels compared with obese subjects without LVH and lean subjects (p<0.05). Adiponectin was negatively correlated with LVMI (R: -0.277, p: 0.002). Furthermore, during the partial correlation analysis where HOMA-IR was controlled, the negative correlation between adiponectin and LVMI progressed (r: -0.283, p: 0.002). The linear regression analysis showed an independent relationship between LVMI and adiponectin. (beta: -0.214, p: 0.01) Obesity is associated with LVH. This study showed direct influence of adiponectin on LVMI.

TGF-beta1 gene polymorphisms and peritoneal equilibration test results in CAPD patients.

Transforming growth factor-beta1 (TGF-beta1) stimulates the expression of collagen mRNA in cultured human peritoneal mesangial cells, which may predispose them to developing peritoneal fibrosis. Polymorphisms in the signal sequence genetically may be responsible for increased TGF-beta1 production (i.e., a substitution at amino acid position 10 and 25, +869 Leu(10)-Pro and +915 Arg(25)-Pro, respectively). The aim of this study was to find out whether there is any relation between peritoneal equilibration test (PET) results and TGF-beta1 gene polymorphism. Thirty-two CAPD patients and 72 healthy subjects were included into the study. Each CAPD patient had undergone two PET with a two-year interval. The patients were classified according to the results of a baseline PET as high (high-high average) and low (low-low average) transporters. In high transporters group (n = 20), the genotype frequencies were found as 45% Leu/Leu, 55% Leu/Pro for codon 10; and 85% Arg/Arg, 15% Arg/Pro for codon 25. In low transporters group (n = 12), the genotype frequencies were detected as 66.7% Leu/Leu and 33.3% Leu/Pro for codon 10; and 83.3% Arg/Arg, 16.7% Arg/Pro for codon 25. The distribution of the TGF-beta1 genotypes in our control population was compatible with a Hardy-Weinberg equilibrium. We found no relation between TGF-beta1 genotypes and peritoneal transport group (chi(2) test, p > 0.5). There was no relation between TGF-beta1 genotype and longitudinal change in peritoneal transport. This study is the first study analyzing the possible link between TGF-betal gene polymorphisms and the characteristics of peritoneal transport and longitudinal change of peritoneal transport characteristics in CAPD patients. Further work is needed to clarify the functional importance of these two polymorphisms in TGF-beta1 production and in the development of peritoneal fibrosis.

Relationship of left ventricular mass to insulin sensitivity and body mass index in healthy individuals.

OBJECTIVE: The objective of this study was to investigate the contribution of insulin resistance, hyperinsulinaemia and obesity, independently of other major factors, to changes in left ventricular mass a cardiovascular risk indicator, in a healthy population without co-morbid states such as diabetes or hypertension. METHODS AND RESULTS: This cross-sectional relational study was perfomed in 153 healthy subjects, comprising 76 men and 77 women with ages ranging from 23 to 67 years. All of them were normotensive and had a normal oral glucose tolerance test, none had cardiovascular disease and none were taking any medication. Weight, height and waist circumference were measured and BMI was calculated. A blood sample was drawn in the fasting state: plasma glucose, insulin, serum total and high density lipoprotein (HDL), low density lipoprotein cholesterol and triglycerides were measured. Insulin resistance was determined by the 'Homeostasis Assessment Model' (HOMA-IR). Subjects were studied by echocardiography. The left ventricular mass was calculated by using the anatomically validated formula of Devereux et al. RESULTS: Left ventricular mass significantly and positively correlated with BMI, age, systolic and diastolic blood pressure and fasting blood glucose. The correlation of left ventricular mass with fasting blood glucose was not maintained after controlling for BMI. BMI, fasting blood glucose, HOMA-IR, systolic and diastolic blood pressure showed significant differences with higher values for people with left ventricular hypertrophy. The logistic regression analysis showed a strong association between left ventricular hypertrophy and BMI (p < 0.05). CONCLUSION: Insulin resistance and fasting insulin is not associated with left ventricular hypertrophy in healthy people, independent of obesity. Obesity appears to be an independent risk factor for left ventricular hypertrophy.